While resting mammalian ventricular myocardium does not usually exhibit pacemaker like activity, under certain conditions spontaneous localized release of Ca2+ from sarcoplasmic reticulum (SR) results in an increase in myoplasmic [Ca2+] (Ca-i) which causes miniature inward currents resulting in oscillations of membrane potential. At the normal resting membrane potential in cardiac myocytes this is insufficient to induce an action potential. However, when spontaneous SR Ca2+ release occurs simultaneously at more than a single locus, i.e. when these loci are "synchronized," the resultant sarcolemmal depolarization is augmented to levels that are sometimes sufficient to produce a spontaneous action potential and contraction. Thus, multiple areas of localized spontaneous Ca2+ release within ventricular cardiac cells, if "synchronized" is a mechanism for abnormal automaticity in these cells and can produce a "heart beat in reverse."